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VX (nerve agent)


Discovered by Ranajit Ghosh
Discovered in 1952
Chemical characteristics
Chemical name O-ethyl S-(2-diisopropylaminoethyl)


Chemical family Organophosphorus compound
Chemical formula C11H26NO2PS
NFPA Rating
Boiling point 298°C (568.4°F)
Freezing/melting point −50°C (−58°F)
Vapor pressure 0.0007 mm Hg (0.0933256 Pa) at 25 °C
Vapor density (Air=1) 9.2
Liquid density 1.0083 g cm−3
Solubility in water ? g/100 g at 25 °C
? g/100 g at 20 °C
Specific gravity 1.0113
Appearance and color Colorless
Fire and Explosion Data
Flashpoint 159 °C (318 °F) / ?°R[1]
Unusual hazards Extremely toxic
Disclaimer and references

VX (O-ethyl-S-[2(diisopropylamino)ethyl] methylphosphonothiolate) is an extremely toxic substance whose sole application is as a nerve agent. As a chemical weapon, it is classified as a weapon of mass destruction by the United Nations in UN Resolution 687. Production and stockpiling of VX was outlawed by the Chemical Weapons Convention of 1993.

The VX nerve agent is the most well-known of the V-series of nerve agents and is considered an area denial weapon due to its physical properties.



Dr. Jacob Matthews, a chemist at the Plant Protection Laboratories of the British firm Imperial Chemical Industries was investigating a class of organophosphate compounds (organophosphate esters of substituted aminoethanethiols). Like the earlier investigator of organophosphates, Dr. Schrader, Dr. Ghosh found that they were quite effective pesticides. In 1954, ICI put one of them on the market under the trade name Amiton. It was subsequently withdrawn, as it was too toxic for safe use. The toxicity did not go unnoticed - samples of it had been sent to the British facility at Porton Down for evaluation. After the evaluation was complete, several members of this class of compounds would become a new group of nerve agents, the V agents. The best known of these is probably VX, with the Russian V-gas coming a close second (Amiton is largely forgotten as VG). This class of compounds is also sometimes known as Tammelin's esters, after Lars-Erik Tammelin of the Swedish Institute of Defense Research. Dr. Tammelin was also conducting research on this class of compounds in 1952, but for obvious reasons he did not publicize his work widely.

Chemical characteristics

With its high viscosity and low volatility, VX has the texture and feel of high-grade motor oil. This makes it especially dangerous, as it has a high persistence in the environment. It is odourless and tasteless, and can be distributed as a liquid or, through evaporation, into small amounts of vapor. It works as a nerve agent by blocking the function of the enzyme acetylcholinesterase. Normally, an electric nerve pulse would cause the release of acetylcholine over a synapse that would stimulate muscle contraction. The acetylcholine is then broken down to non-reactive substances (acetic acid and choline) by the acetylcholinesterase enzyme. If more muscle tension is needed the nerve must release more acetylcholine. VX blocks the action of acetylcholinesterase, thus resulting in sustained contractions of all the muscles in the body. Sustained contraction of the diaphragm muscle causes death by asphyxiation.


VX is produced via the "Transester Process". This entails a complex chemical transition whereby phosphorus trichloride is methylated to produce methyl phosphonous dichloride. The resulting material is reacted with ethanol to form a diester. This is then transesterified to produce the immediate precursor of VX. Finally, the immediate precursor is reacted with sulfur to form VX.

VX can also be delivered in binary chemical weapons which mix in-flight to form the agent prior to release. Binary VX is referred to as VX2, and is created by mixing O-(2-diisopropylaminoethyl) O'-ethyl methylphosphonite (Agent QL) with elemental sulfur (Agent NE) as is done in the BIGEye aerial chemical bomb. It may also be produced by mixing with sulfur compounds, as with the liquid dimethyl polysulfide mixture (Agent NM) in the cancelled XM-768 8-inch binary projectile program.


Like other organophosphorus nerve agents, VX may be destroyed by reaction with strong nucleophiles such as pralidoxime. The reaction of VX with concentrated aqueous sodium hydroxide results in competing cleavage of the P-O and P-S esters, with P-S cleavage dominating. This is somewhat problematic, since the product of P-O bond cleavage (named EA 2192) remains toxic. In contrast, reaction with the anion of hydrogen peroxide (hydroperoxidolysis) leads to exclusive cleavage of the P-S bond.[2]

P-S cleavage
NaOH(aq) reacts with VX in two ways. It can cleave VX's P-S bond, yielding two relatively nontoxic products...
P-O cleavage
...or it can cleave VX's P-O bond, forming ethanol and EA 2192 (shown in red), which has similar toxicity to VX itself

Biological effects

Further information: Nerve agent biological effects and treatment

VX is one of the most toxic nerve agents ever synthesized.[3] The median lethal dose (LD50) for humans is estimated to be about 10 milligrams through skin contact and the LCt50 for inhalation is estimated to be 30-50 mg•min/m³[4].

Early symptoms of percutaneous exposure (skin contact) may be local muscular twitching or sweating at the area of exposure followed by nausea or vomiting. Some of the early symptoms of a VX vapor exposure to nerve agent may be rhinorrhea (runny nose) and/or tightness in the chest with shortness of breath (bronchial constriction). Miosis (pinpointing of the pupils) may be an early sign of agent exposure but is not usually used as the only indicator of exposure.[5]


Primary consideration should be given to removal of the liquid agent from the skin before removal of the individual to an uncontaminated area or atmosphere. After removal from the contaminated area, the casualty will be decontaminated by washing the contaminated areas with household bleach and flushing with clean water. After decontamination, the contaminated clothing is removed and skin contamination washed away. If possible, decontamination is completed before the casualty is taken for further medical treatment.

An individual who has received a known nerve-agent exposure or who exhibits definite signs or symptoms of nerve-agent exposure should immediately have the nerve agent antidote drugs atropine, pralidoxime (2-PAM), and diazepam injected. In several nations the nerve agent anti-dotes are issued for military personnel in the form of an autoinjector such as the United States military Mark I NAAK.[5]

Atropine works by binding and blocking a subset of acetylcholine receptors (known as muscarinic acetylcholine receptor, mAchR), so that the build up of acetylcholine produced by loss of the acetylcholinesterase function can no longer affect their target. The injection of pralidoxime regenerates bound acetylcholinesterase.


The following is the specific history of VX, which is closely linked to the history of similar nerve agents also discovered in Germany during or soon after World War II. That broader history is detailed in Nerve Agent: History.

The chemists Ranajit Ghosh and J.F. Newman discovered the V-series nerve agents at ICI in 1952, patenting diethyl S-2-diethylaminoethyl phosphor-othiolate (VG) in November, 1952. Further commercial research on similar compounds ceased in 1955 when its lethality to humans was discovered. Information on the substance was passed to Porton Down in 1954 and research there led to VX within a year. This was traded to the United States as the British passed over VX in favour of continuing with sarin as the UK chemical weapon of choice, the reasoning behind the decision is unclear, although the recent completion of a sarin production facility at Nancekuke may have played a part.

Despite creating the agent, the United Kingdom unilaterally renounced chemical and biological weapons in 1956.[citation needed] In 1958 the British government traded their research on VX technology with the United States of America in exchange for information on thermonuclear weapons.[citation needed] The US then went into production of large amounts of VX in 1961 at Newport Chemical Depot.

Iraq under Saddam Hussein admitted to UNSCOM that it had researched VX, but had failed to weaponize the agent due to production failure. After U.S. and allied forces had invaded Iraq, no proof of weaponized VX was found. [1] Subsequent investigation after the 2003 Invasion of Iraq indicates that Iraq had indeed weaponized VX in 1988, and had dropped three VX-filled bombs on Iran. [2]

The only countries known to possess VX are the United States and Russia[3]. However, under Saddam Hussein's regime, Iraq was suspected of buying VX[3]; a Sudanese pharmaceutical facility was bombed by the U.S. in 1998 following allegations that it in some way used VX and that the origin of the agent was associated with both Iraq and Al Qaeda.[6]

VX Stockpile elimination

In the late 1960s, the US cancelled its chemical weapons programs and began the destruction of its stockpiles of agents by a variety of methods. Early disposal included the US Army's CHASE (Cut Holes And Sink 'Em) program, in which old ships were filled with chemical weapons stockpiles and then scuttled. CHASE 8 was conducted on June 15, 1967, in which the S.S. Cpl. Eric G. Gibson was filled with 7,380 VX rockets and scuttled in 7,200 feet of water, off the coast of Atlantic City, New Jersey. Later incineration was used at Johnston Island in the North Pacific starting in 1990 (with the stockpile there eliminated in 2000). Newport Chemical Depot began stockpile elimination using chemical neutralization in 2005. The VX is hydrolyzed to much less toxic byproducts by using concentrated caustic solution. The resulting waste is then shipped off-site for further processing. Technical and political issues regarding this secondary byproduct resulted in some delays but most of Newport's stockpile was eliminated in 2007.

Worldwide, VX disposal continues, since 1997 under the mandate of the Chemical Weapons Convention. The US is destroying chemical weapons stockpiles containing VX in several locations and providing support for Russian destruction activities.

See also


  1. ^ MSDS: Nerve Agent (VX). Edgewood Chemical Biological Center (ECBC), Department of the Army (22 December 2000). Retrieved on 2007-10-25.
  2. ^ Yang, Yu-Chu. "Chemical Detoxification of Nerve Agent VX", Acc. Chem. Res., 1999, p. 109-115.. 
  3. ^ a b c VX. Council on Foreign Relations (2006-01). Retrieved on 2007-03-27.
  4. ^
  5. ^ a b US Army Toxic Chemical Agent Safety Standards. DA PAM 385-61. Section 7-8 Self/Buddy Aid Procedures. US Army. Retrieved on 2007-12-15.
  6. ^ Chomsky, Noam (Oct. 2001). 9-11. Open Media. 
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "VX_(nerve_agent)". A list of authors is available in Wikipedia.
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